Characterization of an HIV-infected Promyelocytic Cell Line Previous studies have demonstrated the relative abilities of various HIV isolates to infect different cell lines. Here we describe the abilities of lymphocytropic HIV-IIIB and monocytropic HIV-MN strains to infect the promyelocytic HL-60 cell line and the maintenance of chronically infected cultures of low virus productivity with no apparent loss of viability. Using HIV- directed activation of galactosidase indicator cells (MAGI assay), monolayers of HeLa-CD4-LTR-~-gal cells revealed up to 15% of HL-60 cells were infected and this coculture produced large, multinuclear syncytia. Using p24 antigen ELISA, we observed significant core antigen production by day 12 post-infection for IIIB and by day 20 post-infection for MN. The HL-60/IIIB cultures, by flow cytometric analysis, revealed ability in anti-gp 120 binding, a decrease in anti-CD4 binding, an increase in FMLP receptor activity and that these infected cells were of smaller size and increased granularity. In higher titers of cell-associated virus samples, destruction of the cell monolayer was apparent, whereas little was noted in cell-free virus titers; this suggests a cell-cell virus transmission. Electron microscopy revealed a fusion-like event of cells in infected culture as well as the presence of large cytoplasmic vacuoles of unknown function. In the presence of dibutyryl cAMP, HIV-infected HL-60 cells were differentiated into neutrophil-like cells and this differentiation had no effect on infectivity of cultures. This may represent a useful in vitro model system for the study alterations in HIV-infected inflammatory cells. Future plans include the use of in situ hybridization techniques to detect early neff gene expression as a marker of infection for comparison to standard detection techniques, since studies have suggested tnis gene product, when detected in the absence of late viral proteins, may represent a restricted viral infection incapable of producing infective virus. Also, we plan to select for a clone to establish cultures of 100% infection in order to better study unique functional and morphologic changes characteristic of HIV-infection. Finally, development of a model system to examine cell-cell interactions between HIV-infected cells and endothelial cell cultures is planned. This may help to provide insight to the possibility of a role for HIV-infected cell-mediated tissue destruction in inflammatory processes. Key Words: HIV; HL-60, Inflammation